Cell Biology

Antibiotics: how do they work and what will future drugs target. “The ideal antibiotic interferes with a vital function of bacteria without affecting host cells” Page, Curtis, Sutter Walker & Hoffman (2002). During the 1920’s, when Penicillin was first discovered, antibiotics were recognized as ‘miracle drugs’, but now they are deemed as insignificant. Wainwright, (2007). This essay will cover the mechanism of action within antibiotics and what the future drugs will target.

Rang, Dale, Ritter and Moore, (2003) suggest antibiotics are classified as two main groups known as bactericidal which destroys pathogenic bacteria and bacteriostatic which inhibit the growth of bacteria, resulting in different functions being carried out in the body. There are four main mechanisms of action which antibiotics use to carry out their function. One of the main functions which bactericidal beta lactum antibiotics use is inhibiting cell wall synthesis of bacteria.

They do this by binding to the enzymes which catalyse the building of chains and cross links in the peptidoglycan thereby inhibiting synthesis and resulting in bacterial cell lysis as shown in figure one. Page et al. (2002). Figure 1 In addition, Page et al. (2002) proposes that bacteriostatic antibiotics inhibit protein synthesis of bacteria and this works by binding to a ribosomal 50 S subunit in the bacteria which blocks the initiation step of protein synthesis resulting in the release of an unfinished protein. This stalls the growth of bacteria.

This can be seen in figure two which shows the site of action of bacteriostatic drugs. Also, inhibiting of membrane function within bacterial cells is another way antibiotics attack to destroy the pathogen. This is achieved by the antibiotic binding to cell membrane, altering its properties, making it more permeable which disrupts osmotic balance causing cell lysis. Rang et al. (2003). Figure 2 Lastly, antibiotics which disrupt the nucleic acid synthesis of a pathogen work by inhibiting topoisomerase – an enzyme needed in DNA replication, and this destroys the bacteria. Page et al (2003).

Although antibiotics functioning are admirable, bacteria have become resistant to antibiotics and because of this there are questions regarding the effectiveness of the drugs and what can be done in the future to make them more efficient for targeting pathogens. Bai et al. (2011) discusses a way in which antibiotics can target bacteria cells by inactivating the bacterial RNA polymerase. “Bacterial RNAP [is] an attractive target for the development of anti-bacterial drugs as its inactivation would lead to bacterial cell death” because it is the central enzyme which promotes translation and without translation the cell will deteriorate.

Bai H et al. (2011). Besides RNA polymerase, DD-ligases are another potential target for antibiotics. They catalyse the synthesis of dipeptides in the early stages of the formation of peptidoglycan and so “their function is essential for bacterial growth and specific to bacteria, making them attractive targets for the development of novel antibiotics”. However, some believe that antibiotics will not be as sufficient in the future due to the resistance of bacteria to these drugs. Figure three shows the increase of bacteria resistance to some antibiotics over the years.

Also Levy (1992) talks about how scientist’s advances will soon offer a way to replace antibiotics as “…a time will come when antibiotics as a mode of therapy will be only a fact of historic interest. ” Antibiotics only destroy or inhibit growth of bacteria and with resistance coming to an increased level, the real question is: are the different mechanisms enough to target these pathogens or will this be an end of an era? Bibliography Wainwright, M. (2007). The first miracle drugs: how the sulfa drugs transformed medicine.

Perspectives in Biology and Medicine. 50 (4), pp. 639-642. Page, C, Curtis,M, Sutter, M, Walker, M & Hoffman,B. (2002). Integrated Pharmacology. 2nd ed. Edinburgh: Mosby. pp. 118-123. Page, C, Curtis,M, Sutter, M, Walker, M & Hoffman,B. (2002). Integrated Pharmacology. 2nd ed. Edinburgh: Mosby. Pp. 124-126. Page, C, Curtis,M, Sutter, M, Walker, M & Hoffman,B. (2002). Integrated Pharmacology. 2nd ed. Edinburgh: Mosby. Pp. 129-134. Rang,P, Dale,M, Ritter,M & Moore,K. (2003). Pharmacology. 5th ed. Edinburgh: Elsevier Science. Pp. 620-622.

Rang,P, Dale,M, Ritter,M & Moore,K. (2003). Pharmacology. 5th ed. Edinburgh: Elsevier Science. p627-628. Bai, H, Zhou, Y, Hou, Z, Xue, X, Meng, J, Luo, X. (2011). Targeting bacterial RNA polymerase: promises for future antisense antibiotics development. Infect Disord Drug Targets. 11 (2), pp. 175-187. Levy, S. (1992). The Antibiotic Paradox: How Miracle Drugs Are Destroying the Miracle [Adobe Digital Editions version]. http://www. questia. com/read/98798254/the-antibiotic-paradox-how-miracle-drugs-are-destroying Figure 1: Figure 2: Table 1:

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